Biomedical subjects

C D Swerdlow

Publications and source records attributed to C D Swerdlow.

At least 19 recordsLinked to original sources

PubMed1997

Application of models of defibrillation to human defibrillation data: implications for optimizing implantable defibrillator capacitance.

BACKGROUND: Theoretical models predict that optimal capacitance for implantable cardioverter-defibrillators (ICDs) is proportional to the time-dependent parameter of the strength-duration relationship. The hyperbolic model gives this relationship for average current in terms of the chronaxie (t(c)). The exponential model gives the relationship for leading-edge current in terms of the membrane time constant (tau(m)). We hypothesized that these models predict results of clinical studies of ICD capacitance if human time constants are used. METHODS AND RESULTS: We studied 12 patients with epicardial ICDs and 15 patients with transvenous ICDs. Defibrillation threshold (DFT) was determined for 120-microF monophasic capacitive-discharge pulses at pulse widths of 1.5, 3.0, 7.5, and 15 ms. To compare the predictions of the average-current versus leading-edge-current methods, we derived a new exponential average-current model. We then calculated individual patient time parameters for each model. Model predictions were validated by retrospective comparison with clinical crossover studies of small-capacitor and standard-capacitor waveforms. All three models provided a good fit to the data (r2=.88 to .97, P<.001). Time constants were lower for transvenous pathways (53+/-7 omega) than epicardial pathways (36+/-6 omega) (t(c), P<.001; average-current tau(m), P=.002; leading-edge-current tau(m), P<.06). For epicardial pathways, optimal capacitance was greater for either average-current model than for the leading-edge-current model (P<.001). For transvenous pathways, optimal capacitance differed for all three models (P<.001). All models provided a good correlation with the effect of capacitance on DFT in previous clinical studies: r2=.75 to .84, P<.003. For 90-microF, 120-microF, and 150-microF capacitors, predicted stored-energy DFTs were 3% to 8%, 8% to 16%, and 14% to 26% above that for the optimal capacitance. CONCLUSIONS: Model predictions based on measured human cardiac-muscle time parameter have a good correlation with clinical studies of ICD capacitance. Most of the predicted reduction in DFT can be achieved with approximately 90-microF capacitors.

Defibrillators, Implantable↗

PubMed1997

Programming of implantable cardioverter-defibrillators on the basis of the upper limit of vulnerability.

BACKGROUND: A patient-specific measure of defibrillation efficacy that requires a minimum number of ventricular fibrillation (VF) episodes would be valuable for programming implantable cardioverter-defibrillators (ICDs). The upper limit of vulnerability (ULV) is the weakest shock strength at or above which VF is not induced when a stimulus is delivered during the vulnerable phase of the cardiac cycle. It correlates with the defibrillation threshold (DFT) and can be determined with a single episode of VF. The objective of this study was to test the hypothesis that ICDs programmed on the basis of the ULV convert spontaneous ICD-detected VF reliably. METHODS AND RESULTS: We studied 100 consecutive patients at ICD implantation and during follow-up of 20 +/- 7 months. At implantation, the ULV and DFT were determined, and the ICD system was tested at a shock strength equal to the ULV + 3 J. During follow-up, the strength of the first shock was programmed to the ULV + 5 J for arrhythmias detected in the VF zone (cycle length < 292 +/- 17 ms). We reviewed stored detection intervals and electrograms from spontaneous episodes of ICD-detected VF to determine the success rate for appropriate first shocks. The programmed first-shock strength was 17.5 +/- 5.2 J. During follow-up, there were 120 appropriate first shocks in 37 patients. The arrhythmia was rapid monomorphic ventricular tachycardia (VT) in 70% of episodes (31 patients), VF in 11% (13 patients), polymorphic VT in 1%, and unclassified in 17% (15 patients). The first shock was successful in 119 of 120 episodes (99%; 95% CI, 93% to 100%). One unclassified episode required two shocks. No patient had syncope associated with an ICD shock or arrhythmic death. CONCLUSIONS: ICD shocks can be programmed on the basis of the ULV, a measurement made in regular rhythm, without a direct measure of defibrillation efficacy.

Aged↗

PubMed1997

Atypical atrioventricular node reciprocating tachycardia masquerading as tachycardia using a left-sided accessory pathway.

OBJECTIVES: The study was performed to document that atrioventricular node reciprocating tachycardia (AVNRT) can be associated with eccentric retrograde left-sided activation, masquerading as tachycardia using a left accessory pathway. BACKGROUND: The eccentric retrograde left-sided activation during tachycardia is thought to be diagnostic of the presence of a left free wall accessory pathway. However, it is not known whether AVNRT can occur with eccentric retrograde left-sided activation. METHODS: We studied 356 patients with AVNRT who underwent catheter ablation. Retrograde atrial activation during tachycardia and ventricular pacing were determined by intracardiac recordings, including the use of a decapolar coronary sinus catheter. RESULTS: The retrograde atrial activation was eccentric in 20 patients (6%). Eight of these patients had the earliest retrograde atrial activation recorded in the lateral coronary sinus leads, and 12 had the earliest retrograde atrial activation recorded in the posterior coronary sinus leads, with the most proximal coronary sinus electrode pair straddling the coronary sinus orifice. These tachycardias were either the fast-slow or the slow-slow form of AVNRT. The slow-fast form of AVNRT was also inducible in 17 of the 20 patients. Successful ablation of the slow pathway in the right atrial septum near the coronary sinus ostium prevented the induction and clinical recurrence of reciprocating tachycardia in all patients. CONCLUSIONS: Atypical AVNRT with eccentric retrograde left-sided activation was demonstrated in 6% of all patients with AVNRT masquerading as tachycardia using a left-sided accessory pathway. Ablation of the slow pathway at the posterior aspects of the right atrial septum resulted in a cure in these patients.

Adult↗

PubMed1997

The zone of vulnerability to T wave shocks in humans.

INTRODUCTION: Shocks during the vulnerable period of the cardiac cycle induce ventricular fibrillation (VF) if their strength is above the VF threshold (VFT) and less than the upper limit of vulnerability (ULV). However, the range of shock strengths that constitutes the vulnerable zone and the corresponding range of coupling intervals have not been defined in humans. The ULV has been proposed as a measure of defibrillation because it correlates with the defibrillation threshold (DFT), but the optimal coupling interval for identifying it is unknown. METHODS AND RESULTS: We studied 14 patients at implants of transvenous cardioverter defibrillators. The DFT was defined as the weakest shock that defibrillated after 10 seconds of VF. The ULV was defined as the weakest shock that did not induce VF when given at 0, 20, and 40 msec before the peak of the T wave or 20 msec after the peak in ventricular paced rhythm at a cycle length of 500 msec. The VFT was defined as the weakest shock that induced VF at any of the same four intervals. To identify the upper and lower boundaries of the vulnerable zone, we determined the shock strengths required to induce VF at all four intervals for weak shocks near the VFT and strong shocks near the ULV. The VFT was 72 +/- 42 V, and the ULV was 411 +/- V. In all patients, a shock strength of 200 V exceeded the VFT and was less than the ULV. The coupling interval at the ULV was 19+/- 11 msec shorter than the coupling interval at the VFT (P < 0.001). The vulnerable zone showed a sharp peak at the ULV and a less distinct nadir at the VFT. A 20-msec error in the interval at which the ULV was measured could have resulted in underestimating it by a maximum of 95 +/- 31 V. The weakest shock that did not induce VF was greater for the shortest interval tested than for the longest interval at both the upper boundary (356 +/- 108 V vs 280 +/- 78 V; P < 0.01) and lower boundary (136 +/- 68 msec vs 100 +/- 65 msec; P < 0.05). CONCLUSIONS: The human vulnerable zone is not symmetric with respect to a single coupling interval, but slants from the upper left to lower right. Small differences in the coupling interval at which the ULV is determined or use of the coupling interval at the VFT to determine the ULV may result in significant variations in its measured value. An efficient strategy for inducing VF would begin by delivering a 200-V shock at a coupling interval 10 msec before the peak of the T wave.

Aged↗

PubMed1997

Upper limit of vulnerability predicts chronic defibrillation threshold for transvenous implantable defibrillators.

INTRODUCTION: The upper limit of vulnerability (ULV) is the shock strength at or above which ventricular fibrillation cannot be induced when delivered in the vulnerable period. It correlates acutely with the acute defibrillation threshold (DFT) and can be determined with a single episode of fibrillation. The goal of this prospective study was to determine the relationship between the ULV and the chronic DFT. METHODS AND RESULTS: We studied 40 patients at, and 3 months after, implantation of transvenous cardioverter defibrillators. The ULV was defined as the weakest biphasic shock that failed to induce fibrillation when delivered 0, 20, and 40 msec before the peak of the T wave. patients were classified as clinically stable or unstable based on prospectively defined criteria. There were no significant differences between the group means for the acute and chronic determinations of ULV (13.5 +/- 5.3 J vs 12.4 +/- 6.8 J, P = 0.25) and DFT (10.1 +/- 5.0 J vs 9.9 +/- 5.7 J, P = 0.74). Five patients (15%) were classified as unstable. The strength of the correlation between acute ULV and acute DFT (r = 0.74, P < 0.001) was similar to that between the chronic ULV and chronic DFT (r = 0.82, P < 0.001). There was a correlation between the change in ULV from acute to chronic and the corresponding change in DFT (r = 0.67, P < 0.001). The chronic DFT was less than the acute ULV +3 J in all 35 stable patients, but it was greater in 2 of 5 unstable patients (P = 0.04). CONCLUSIONS: The strength of the correlation between the chronic ULV and the chronic DFT is comparable to that between the acute ULV and the acute DFT. Temporal changes in the ULV predict temporal changes in the DFT. In clinically stable patients, a defibrillation safety margin of 3 J above the acute ULV proved an adequate chronic safety margin.

Aged↗

PubMed1996

Charge-burping theory correctly predicts optimal ratios of phase duration for biphasic defibrillation waveforms.

BACKGROUND: For biphasic waveforms, it is accepted that the ratio of the duration of phase 2 to the duration of phase 1 (phase-duration ratio) should be < or = 1. The charge-burping theory postulates that the beneficial effects of phase 2 are maximal when it completely removes the charge delivered by phase 1. It predicts that the phase-duration ratio should be < 1 when the time constant of the defibrillation system (tau s) exceeds the time constant of the cell membrane (tau m) but > 1 when tau s < tau m. This study tested the hypothesis that the optimal phase-duration ratio depends on tau s (the product of the defibrillator capacitance and pathway resistance). METHODS AND RESULTS: In a canine model of transvenous defibrillation (n = 8), we determined stored-energy defibrillation thresholds (DFTs) for biphasic waveforms from conventional capacitors (140 microF. tau s = 7.1 +/- 0.8 ms) and very small capacitors (40 microF. tau s = 2.0 +/- 0.2 ms). Each capacitance was tested with phase-duration ratios of 0.5, 1, 2, and 3. The duration of phase 1 approximated the optimal monophasic waveform, 6.3 +/- 0.7 ms for 140-microF waveforms and 2.8 +/- 0.2 ms for 40-microF waveforms. For 140-microF waveforms, the DFT was lower for phase-duration ratios < or = 1 than for phase-duration ratios > 1 (P = .0003). The reverse was true for 40-microF capacitors (P = .0008). There was a significant interaction between the effects of capacitance and phase-duration ratio on DFT (P = .0002). The lowest DFT for 40-microF waveforms was less than the lowest DFT for 140-microF waveforms (4.9 +/- 2.5 versus 6.4 +/- 2.4 J, P < .05). CONCLUSIONS: The optimal phase-duration ratio is < or = 1 for conventional capacitors and > 1 for small capacitors. This supports the predictions of the charge-burping theory.

Animals↗

PubMed1996

Upper limit of vulnerability is a good estimator of shock strength associated with 90% probability of successful defibrillation in humans with transvenous implantable cardioverter-defibrillators.

OBJECTIVES: The goals of this study were to determine the probability of successful defibrillation at the upper limit of vulnerability and to evaluate a minimal safety margin for implantable cardioverter-defibrillator first shocks based solely on the upper limit of vulnerability. BACKGROUND: The upper limit of vulnerability is the strength at or above which ventricular fibrillation is not induced when a stimulus is delivered during the vulnerable phase of the cardiac cycle. It has been proposed as an estimate of defibrillation efficacy because it correlates with the defibrillation threshold and can be determined with a single episode of fibrillation. METHODS: We studied 40 patients prospectively at implantation of transvenous cardioverter-defibrillators. Defibrillation threshold was defined as the weakest biphasic shock that defibrillated after 10 s of ventricular fibrillation. The upper limit of vulnerability was defined as the weakest biphasic shock that did not induce ventricular fibrillation when given at 0, 20 and 40 ms before the peak of the T wave in ventricular paced rhythm at cycle length 500 ms. After determination of the upper limit of vulnerability and defibrillation threshold, patients underwent six additional fibrillation-defibrillation episodes. The strength of five of the defibrillation shocks was equal to the upper limit of vulnerability; the strength of one of the six shocks was randomly selected to be equal to the upper limit of vulnerability plus 3 J. The implantable cardioverter-defibrillator was tested at the upper limit of vulnerability plus 3 J in 28 patients. RESULTS: The defibrillation threshold was 8.8 +/- 5.0 J (mean +/- SD), and upper limit of vulnerability was 11.3 +/- 4.6 J; the defibrillation threshold and upper limit of vulnerability were highly correlated (r = 0.89, p < 0.001). The success rate for the 200 defibrillation shocks with strength equal to the upper limit of vulnerability was 90% (95% confidence intervals based on proportion of successes in 40 patients: 86% to 94%). All five defibrillation test shocks at the upper limit of vulnerability were successful in 24 patients (60%); four of five were successful in 12 patients (30%); and three of five were successful in 4 patients (10%). All 40 test shocks and 28 implantable cardioverter-defibrillator shocks with a strength equal to the upper limit of vulnerability plus 3 J were successful. CONCLUSIONS: The upper limit of vulnerability is a good estimator of the shock strength associated with 90% probability of successful defibrillation (DFT90). A strength of 3 J above the upper limit of vulnerability is a good estimate of the minimal acute safety margin for implantable cardioverter-defibrillator first shocks.

Adult↗

PubMed1996

Comparative reproducibility of defibrillation threshold and upper limit of vulnerability.

The upper limit of vulnerability (ULV) is the strength at or above which VF is not induced when a stimulus is delivered during the vulnerable phase of the cardiac cycle. Previous studies have demonstrated a statistically significant correlation between the ULV and the defibrillation threshold (DFT) in groups of patients. However, the correlation between ULV and DFT may not be close in individual patients. This imperfect correlation may be due to physiological factors or to limitations of the measurement methods. The reproducibility of either DFT or ULV has not been studied critically. The purpose of this study was to compare the reproducibility of clinically applicable methods for determination of DFT and ULV. We prospectively studied 25 patients with a transvenous implantable cardioverter defibrillator (Medtronic 7219D) at postoperative electrophysiological study. DFT was defined as the lowest energy that defibrillated after 10 seconds of VF. The ULV was defined as the lowest energy that did not induce VF with three shocks at 0, 20, and 40 ms before the peak of the T wave in ventricular paced rhythm at a cycle length of 500 ms. Both the DFT and the ULV were determined twice for biphasic pulses using a three-step, midpoint protocol. There was no significant difference between the two determinations of DFT (10.1 +/- 5.9 J vs 10.4 +/- 5.8 J), the two determinations of ULV (13.4 +/- 6.8 J vs 13.8 +/- 6.6) or the DFT-ULV Pearson correlation coefficients for each determination (0.84, P < 0.001 vs 0.75, P < 0.001). To analyze reproducibility, Lin concordance coefficients for second determination versus first determination were constructed for both ULV and DFT. This coefficient is similar to the Pearson correlation coefficient, but measures closeness to the line of identity rather than the line of regression. The Lin concordance coefficient for ULV was higher than that for DFT (0.93, 95% CI 0.85-0.97 vs 0.64, 95% CI 0.33-0.82; P < 0.01). For paired comparison of defibrillation efficacy under different experimental conditions, the sample sizes required to detect differences of 2 J, 3 J, and 4 J (80% power, P < 0.05) were 52, 24, and 15 for DFT versus 15, 8, and 6 for ULV. We conclude that a simple, clinically applicable method for determination of ULV is more reproducible than the single point DFT. Measured correlations between the ULV and single point are limited by the reproducibility of the DFT measurement.

Defibrillators, Implantable↗

PubMed1996

Short biphasic pulses from 90 microfarad capacitors lower defibrillation threshold.

For defibrillation between right ventricular and retropectoral patch electrodes using truncated exponential pulses, the stored energy defibrillation threshold (DFT) is lower for short pulses from small 60-microF capacitors than for conventional pulses from 120-microF capacitors, but 60-microF pulses frequently require higher voltages than are currently used. The goal of this study was to determine if DFT could be reduced by intermediate size 90-microF capacitors. This study compared biphasic waveform DFTs for 120 microF-65% tilt pulses, 90 microF-65% tilt pulses, and 90 microF-50% tilt pulses in 20 patients at defibrillator implantation. The 90 microF-50% tilt pulses were selected because their duration is half that of 120 microF-65% tilt pulses. The stored energy DFT for 90 microF-50% tilt pulses (9.1 +/- 4.3 J) was less than both the DFT for 120 microF-65% tilt pulses (12.0 +/- 5.5 J, P < 0.005) and the DFT for 90 microF-65% tilt pulses (11.6 +/- 5.8 J, P < 0.005). There was no significant difference between the latter two values. The voltage DFTs for 90 microF-50% pulses (436 +/- 113 V) and 120 microF-65% tilt pulses (436 +/- 104 V) were not statistically different; the voltage DFT for 90 microF-65% tilt pulses was higher than for either of the other two pulses (490 +/- 131, P < 0.005). The DFT was 20 J or greater in three patients for both 120 microF-65% tilt pulses and 90 microF-65% tilt pulses, but it was 16 J or less in all patients for 90 microF-50% tilt pulses. When pathways were dichotomized by the median resistance of 71 omega, 90 microF-50% tilt pulses significantly reduced DFTs compared to 120 microF-65% tilt pulses for higher resistance pathways (9.2 +/- 4.0 J vs 13.0 +/- 6.2 J, P = 0.002), but not lower resistance pathways (9.0 +/- 4.8 J vs 10.9 +/- 4.6 J, P = NS). For the electrode configuration tested, biphasic 90 microF-50% tilt pulses reduce stored energy DFT in comparison with 120 microF-65% tilt pulses without increasing voltage DFT. However, 90 microF-65% tilt pulses provide no benefit.

Defibrillators, Implantable↗

PubMed1995

Optimal electrode configuration for pectoral transvenous implantable defibrillator without an active can.

A new 83 cm3 implantable cardioverter-defibrillator (ICD) designed for pectoral implantation has been implanted most frequently using right ventricular and superior vena cava (RV-->SVC) electrodes; a patch electrode (RV-->patch + SVC) has been added when necessary to decrease the defibrillation threshold (DFT). The goal of this prospective study was to compare biphasic waveform DFTs for 3 electrode configurations: RV-->patch, RV-->SVC, and RV-->patch + SVC in 25 consecutive patients. The patch was positioned in a left retro-pectoral pocket, and the SVC electrode was positioned with the tip at the junction of the SVC and innominate vein. In the first 15 patients, all 3 electrode configurations were tested in random order; in the last 10 patients, only the RV-->patch and RV-->patch + SVC configurations were tested. In the first 15 patients, the stored-energy DFT for the RV-->SVC configuration (15.2 +/- 7.7 J) was higher (p < 0.001) than the DFT for the RV-->patch configuration (11.3 +/- 6.2 J) and the RV-->patch + SVC configuration (10.0 +/- 5.8 J). For all 25 patients, the DFT was lower for the RV-->patch + SVC configuration (9.7 +/- 5.1 J) than for the RV-->patch configuration (12.4 +/- 6.6 J, p = 0.005). The pathway resistance was highest for the RV-->patch configuration (72 +/- 9 omega), lower for the RV-->SVC configuration (63 +/- 6 omega, p < 0.01), and lowest for the RV-->patch + SVC configuration (46 +/- 3 omega, p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed1995

Arrhythmias after cardioverter-defibrillator implantation: comparison of epicardial and transvenous systems.

Surgery for implantable cardioverter-defibrillators can cause postoperative exacerbation of ventricular and atrial arrhythmias. It is not known whether the techniques of electrode implantation (epicardial vs transvenous) influence the incidence of arrhythmia exacerbation. We reviewed the postoperative course of 229 consecutive patients who received either epicardial (n = 119) or transvenous (n = 110) implantations from 1984 to 1994. Exacerbation of ventricular tachycardia (VT) was defined as an increase in the number of sustained VTs during the postoperative versus the preoperative 2 weeks. Of the entire cohort, 18 patients (8%) developed exacerbation of VT after operation, which was more frequent in patients with epicardial than with transvenous implantations (12% vs 4%, p < 0.03, odds ratio 3.5, 95% confidence interval 1.0 to 13.2). New-onset atrial fibrillation occurred in 15% of patients with epicardial versus 1% of those with transvenous implantations (p = 0.00005, odds ratio 19.4, 95% confidence interval 2.7 to 86.7). These differences persisted after excluding patients with concurrent cardiac surgery. Preoperative occurrence of arrhythmias was the strongest independent predictor for postoperative occurrence (p < 0.01 for VT, p < 0.0001 for atrial fibrillation). Epicardial implantation (p = 0.03) and a history of myocardial infarction (p = 0.04) were independent predictors for postoperative VT exacerbation, whereas epicardial implantation (p < 0.05) and concurrent coronary bypass surgery (p = 0.0001) were independent predictors for postoperative new atrial fibrillation. Perioperative discontinuation of antiarrhythmic drugs did not influence postoperative VT exacerbation. Epicardial implantation was associated with longer length of hospital stay than transvenous implantation (p = 0.0005), independent of age, left ventricular ejection fraction, and concurrent cardiac surgery.

Aged↗

PubMed1994

Effects of voltage and respiration on impedance in nonthoracotomy defibrillation pathways.

The effects of applied voltage and phase of respiration on impedance of pathways used by implantable cardioverter-defibrillators were investigated. Patients were studied at implantation of cardioverter-defibrillators using epicardial (n = 12) or transvenous and subcutaneous (SQ) (n = 30) electrodes. Transvenous-SQ pathways were right ventricular cathode to SQ anode and coronary sinus cathode to SQ anode. Transvenous-transvenous pathways were right ventricle to coronary sinus and right ventricle to superior vena cava. Patients with nonthoracotomy electrode systems were studied at end-expiration and end-inspiration. Five shocks of 65 to 745 V (0.2 to 34 J) were given in random order in sinus rhythm. Over this range, end-expiratory impedance decreased monotonically for all pathways. This effect was greatest for transvenous-SQ pathways (13 +/- 3% to 17 +/- 4%, p < 0.001), intermediate for transvenous-transvenous pathways (5 +/- 4% to 8 +/- 5%, p < 0.001), and least for epicardial pathways (3 +/- 3%, p = 0.006). Paired data in inspiration and expiration showed that inspiration increased impedance in transvenous-SQ pathways (p < 0.001) but not in transvenous-transvenous pathways. Further, the effects of respiration and voltage on impedance in transvenous-SQ pathways were interactive (p < 0.001): Inspiration increased voltage-dependence of impedance. The magnitude of the inverse relationship between voltage and impedance depends on type of defibrillation pathway. The effect of respiration on impedance suggests that voltage-dependence of impedance is greatest in the lungs. These findings have potential relevance for intraoperative testing of cardioverter-defibrillators and selection of pathways for low-energy cardioversion.

Aged↗

PubMed1994

Underdetection of ventricular tachycardia by algorithms to enhance specificity in a tiered-therapy cardioverter-defibrillator.

OBJECTIVES: The goal of this study was to determine the incidence and clinical significance of underdetection in 125 patients treated with a tiered-therapy cardioverter-defibrillator, the Medtronic PCD. BACKGROUND: Underdetection, distinct from undersensing, is a unique, potential complication of new algorithms that enhance specificity in tiered-therapy cardioverter-defibrillators. These algorithms may delay or prevent recognition of ventricular tachycardia even though electrograms are sensed accurately and RR intervals meet the programmed interval criterion. METHODS: Underdetection was defined as delay in detection > 5 s at electrophysiologic study or symptomatic delay or detection failure at follow-up of 15 +/- 8 months. RESULTS: We identified six specific mechanisms of underdetection caused by algorithms to discriminate sustained ventricular tachycardia from sinus tachycardia, atrial fibrillation, ventricular fibrillation and nonsustained ventricular tachycardia. Underdetection caused detection delays in 13 (1.9%) of 677 induced ventricular tachyarrhythmia episodes in 12 patients (9.6%). During follow-up, underdetection occurred in 7 (9.9%) of 71 patients in whom ventricular tachycardia therapies were programmed. Failure to detect ventricular tachycardia occurred in 6 (0.6%) of 988 spontaneous ventricular tachycardia episodes in four patients (5.6%); 2 episodes required external cardioversion. After defibrillator reprogramming, underdetection did not occur. CONCLUSIONS: Algorithms to enhance specificity cause underdetection of ventricular tachycardia in a significant minority of patients with tiered-therapy cardioverter-defibrillators. Optimal programming can minimize underdetection.

Algorithms↗

PubMed1994

Discrimination of ventricular tachycardia from sinus tachycardia and atrial fibrillation in a tiered-therapy cardioverter-defibrillator.

OBJECTIVES: This study was conducted to evaluate criteria for discrimination of ventricular tachycardia from atrial fibrillation and sinus tachycardia in a tiered-therapy cardioverter-defibrillator (Medtronic PCD). BACKGROUND: Interval stability algorithms discriminate ventricular tachycardia from atrial fibrillation. Onset algorithms discriminate ventricular tachycardia from sinus tachycardia. Neither has been validated clinically. METHODS: The stability criterion requires that a ventricular tachycardia interval not vary from any of the three previous intervals by more than the programmable stability value. The onset criterion detects initiation of ventricular tachycardia only if the ratio of an interval to the mean of four previous intervals is less than a programmed onset ratio and either the second or third preceding interval exceeds the ventricular tachycardia detection interval. We evaluated these criteria in 100 patients at electrophysiologic study and exercise testing (65 patients) and during a mean (+/- SD) follow-up of 16.2 +/- 7.9 months. The PCDs were programmed to tiered therapy in 54 patients. In the remaining 46 patients, the PCD's memory for detected ventricular tachycardia was used to study the specificity of the chosen onset criterion for rejecting sinus tachycardia. We used stored intervals preceding appropriate (n = 99) and inappropriate (n = 54) detections to test a new onset criterion that was less sensitive to a single index interval. RESULTS: Programmed stability of 40 ms decreased detection of induced atrial fibrillation by 95% (20 patients), paroxysmal atrial fibrillation by 95% (6 patients) and chronic atrial fibrillation by 99% (9 patients); all episodes of spontaneous (n = 877) and induced (n = 339) ventricular tachycardia were detected. A programmed onset ratio of 87% rejected sinus acceleration (98%) but caused underdetection of 0.5% of ventricular tachycardias. The onset criterion permitted inappropriate detection of premature ventricular complexes during sinus tachycardia, but the new criterion reduced these inappropriate detections by 98%. CONCLUSIONS: The PCD's onset and stability criteria reduced inappropriate detection of atrial fibrillation and sinus acceleration while detecting 99.5% of ventricular tachycardias.

Aged↗

PubMed1994

Effect of capacitor size and pathway resistance on defibrillation threshold for implantable defibrillators.

BACKGROUND: The time constant of truncated exponential pulses used with implantable defibrillators is determined by the output capacitor size and defibrillation pathway resistance. The optimal capacitor size is unknown. METHODS AND RESULTS: This study compared defibrillation threshold (DFT) for standard 120-microF capacitors (DFT120) and smaller 60-microF capacitors (DFT60) at implantation of cardioverter-defibrillators in 67 patients using epicardial electrodes (15 patients) or one of four transvenous electrode configurations (52 patients). Paired comparisons of DFT60 and DFT120 were made for 44 defibrillation pathways using monophasic pulses and for 53 pathways using biphasic pulses. Truncated exponential pulses with 65% tilt were used. Pooled data from all electrode configurations showed a significant inverse correlation between pathway resistance and the ratio of stored energy DFT60 to DFT120 (monophasic pulses: r = .75, P = .0001; biphasic pulses: r = .68, P = .0001). Data from all electrode configurations formed a continuum with 120-microF capacitors superior for low-resistance pathways and 60-microF capacitors superior for high-resistance pathways. For pathways with resistance < or = 40 omega, the modest advantage of 120-microF capacitors applied primarily to pathways with low DFTs: 8.2 +/- 6.1 versus 9.6 +/- 5.4 J (P = .001) for monophasic pulses and 4.1 +/- 2.8 versus 5.1 +/- 3.1 J (P < .02) for biphasic pulses. The greater advantage of 60-microF capacitors for pathways with resistance > or = 61 omega applied to pathways with higher DFTs: 12.4 +/- 4.3 versus 23.1 +/- 6.4 J (P = .0001) for monophasic pulses and 8.5 +/- 4.9 versus 12.5 +/- 6.4 J (P = .0001) for biphasic pulses. For pathways using monophasic 120-microF pulses versus 95% for 60-microF pulses. Similarly, the DFT was < or = 10 J for 48% of pathways using biphasic 120-microF capacitors versus 83% for 60-microF pulses. CONCLUSIONS: In comparison with conventional 120-microF capacitors, 60-microF capacitors had clinically insignificant higher DFTs for low-resistance pathways and clinically important lower DFTs for high-resistance pathways. Optimal capacitance is inversely related to pathway resistance for clinical defibrillation pathways and waveforms.

Aged↗

PubMed1994

Upper limit of vulnerability reliably predicts the defibrillation threshold in humans.

BACKGROUND: The upper limit of vulnerability is the stimulus strength above which electrical stimulation cannot induce ventricular fibrillation even when the stimulus occurs during the vulnerable period of the cardiac cycle. The purpose of this study was to test the hypothesis that the upper limit of vulnerability can accurately predict the defibrillation threshold in patients undergoing implantable cardioverter-defibrillator (ICD) implantation using nonthoracotomy lead systems. METHODS AND RESULTS: We studied 77 patients at the time of ICD implantation. Multiple endocardial-endocardial and endocardial-subcutaneous shock pathways were used. Two different protocols were used to test the upper limit of vulnerability. In protocol 1 (n = 17), the upper limit of vulnerability was tested with two shocks on the peak or the up-slope of the T wave of paced rhythm. The shocks were given randomly either at the peak and 20 milliseconds before the peak of T wave (n = 7) or at 20 and 40 milliseconds before the peak of T wave (n = 10). In protocol 2 (n = 60), the upper limit of vulnerability was tested with three shocks delivered at 0, 20, and 40 milliseconds before the peak of the T wave. The weakest shock that failed to induce ventricular fibrillation by a 5-J step-down or step-up method was defined as the upper limit of vulnerability. The defibrillation threshold was also determined by a 5-J step-down or step-up method. In protocol 1, the upper limit of vulnerability (9 +/- 6 J) was significantly lower than the defibrillation threshold (13 +/- 7 J) with a correlation coefficient of .87 and P < .001. In protocol 2, the upper limit of vulnerability (13 +/- 6 J) was not significantly different from the defibrillation threshold (13 +/- 6 J) with a correlation coefficient of .85 and P < .001. In 45 of the 60 patients, the upper limit of vulnerability was < or = 15 J; all had a defibrillation threshold of < or = 20 J. In 51 of the 60 patients, the upper limit of vulnerability was within 5 J of the defibrillation threshold. The upper limit of vulnerability overestimated the defibrillation threshold by > 10 J in 8 patients and underestimated the defibrillation threshold by > 10 J in only 1 patient. The overestimation and underestimation occurred only in patients with the upper limit of vulnerability > 15 J. CONCLUSIONS: When tested with three shocks on and before the peak of the T wave, the upper limit of vulnerability accurately predicted the defibrillation threshold in patients undergoing ICD implantation using nonthoracotomy lead systems. This method required either one or no episodes of ventricular fibrillation in most patients.

Aged↗

PubMed1993

Relation between upper limit of vulnerability and defibrillation threshold in humans.

BACKGROUND: In the canine model, an upper limit of shock strength exists that can induce ventricular fibrillation during the vulnerable period of the cardiac cycle. This shock strength (the upper limit of vulnerability) closely correlates with the defibrillation threshold and supports the "upper limit of vulnerability" hypothesis of defibrillation. It is not known whether an upper limit of vulnerability exists in humans or whether this limit correlates with the defibrillation threshold. METHODS AND RESULTS: In 13 patients undergoing implantable cardioverter-defibrillator implantation, the shock strengths associated with a 50% probability of reaching the upper limit of vulnerability (ULV50) and a 50% probability of reaching the defibrillation threshold (DFT50) were determined by the up-down algorithm. The ULV50 was determined only for the mid-upslope of the positive T waves and for the mid-downslope of the negative T waves. No major complications occurred during surgery. An upper limit of vulnerability was demonstrated in each patient. The ULV50 was 300 +/- 138 V or 6.8 +/- 5.8 J, which was significantly lower than the DFT50 of 347 +/- 167 V (p = 0.038) or 9.1 +/- 7.3 J (p = 0.013). The correlation between the ULV50 and the DFT50 was significant (r = 0.90, p < 0.001 for voltage; r = 0.93, p < 0.001 for energy). CONCLUSIONS: An upper limit of vulnerability is present in humans. There is a significant correlation between the ULV50 and the DFT50, and the ULV50 is significantly lower than the DFT50.

Algorithms↗

PubMed1990

Long-term outcome in patients who survive out of hospital ventricular fibrillation and undergo electrophysiologic studies: evaluation by electrophysiologic subgroups.

The long-term outcome of 241 survivors of out of hospital ventricular fibrillation who underwent programmed electrical stimulation was evaluated. Patients were categorized according to the rhythm induced at baseline drug-free electrophysiologic testing. Ventricular fibrillation was induced in 39 patients (16%) (Group 1), sustained ventricular tachycardia in 66 patients (27%) (Group 2) and nonsustained ventricular tachycardia in 34 patients (14%) (Group 3); 102 patients (42%) (Group 4) did not have an arrhythmia inducible at baseline electrophysiologic testing. Antiarrhythmic drugs were administered over the long term to 92% of patients in Group 2, 91% of patients in Group 1 and 47% of patients in Group 4. At a mean follow-up time of 30 +/- 15 months, recurrent sudden cardiac death or nonfatal ventricular fibrillation occurred in 11 (28%) of 39 patients with inducible ventricular fibrillation (Group 1), 14 (21%) of 66 patients with inducible sustained ventricular tachycardia (Group 2), 4 (12%) of 34 patients with inducible nonsustained ventricular tachycardia (Group 3) and 16 (16%) of 102 patients without inducible arrhythmias (Group 4). Actuarial analysis revealed a 2 year cumulative arrhythmia-free survival rate of 65% for patients in Group 2, 71% for patients in Group 1, 79% for patients in Group 3 and 81% for patients in Group 4 (p = 0.02). Actuarial survival of patients with inducible sustained ventricular tachycardia or ventricular fibrillation suppressed by electrophysiologically guided drug therapy was not significantly different from that in patients whose arrhythmia was not suppressed. Multivariate regression analysis revealed that only the presence of congestive heart failure was an independent predictor of outcome in these patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Anti-Arrhythmia Agents↗